Downregulation of water channel aquaporin-4 in rats with experimental autoimmune encephalomyeritis induced by myelin basic protein

详细信息    查看全文

• 作者：Tomoki Kaneyama^a ; ¹ ; Sho Takizawa^b ; Sayaka Tsugane^b ; Satoshi Yanagisawa^b ; Naoya Takeichi^b ; Takashi Ehara^a ; Motoki Ichikawa^b ; Chang-Sung Koh^b ; ^{kshosei@shinshu-u.ac.jp}
• 关键词：Aquaporin-4 (AQP4) ; Myelin basic protein (MBP) ; Experimental autoimmune encephalomyelitis (EAE) ; Neuromyelitis optica (NMO) ; Glial fibrillary acidic protein (GFAP)
• 刊名：Cellular Immunology
• 出版年：2013
• 出版时间：January, 2013
• 年：2013
• 卷：281
• 期：1
• 页码：91-99
• 全文大小：1998 K

文摘

Characteristics of myelin basic protein (MBP)-induced experimental autoimmune encephalomyelitis (EAE) include acute edema and infiltration of mononuclear cells (MNCs) in the microvessels of central nervous system (CNS). Aquaporin-4 (AQP4) is a water channel protein expressed in astrocytes foot process throughout the CNS. We performed immunostaining, western blotting and semi-quantitative real-time RT-PCR of AQP4 and glial fibrillary acidic protein (GFAP) in CNS from rats immunized with MBP. Immunohistochemical analysis revealed that AQP4 is down-regulated in MNCs infiltrated microvessels of rats with EAE. Furthermore, western blotting and real-time RT-PCR analyses showed that AQP4 was significantly decreased at the stage of severe EAE compared with control rats. On the other hand, expression of GFAP-protein was significantly increased after stage of severe EAE. Our findings suggest that AQP4 may be involved in forming edema in the inflammatory lesions of EAE accompanying with up-regulation of reactive astrocyte.